Arterial blood pressure is defined as lateral pressure exerted by column of blood on the wall of arteries. This pressure is exerted when blood flows through the arteries.

Generally, the term blood pressure refers to arterial blood pressure. Arterial blood pressure is expressed in four different terms.

1. Systolic Blood Pressure

Systolic blood pressure or systolic pressure is defined as the maximum pressure exerted in arteries during systole of heart.

2. Diastolic Blood Pressure

Diastolic blood pressure or diastolic pressure is defined as the minimum pressure in arteries during diastole of heart.

3. Pulse Pressure

Pulse pressure is the difference between systolic pressure and diastolic pressure.

4. Mean Arterial Blood Pressure

It is the average pressure existing in arteries. It is not the arithmetic mean of systolic and diastolic pressures. It is the diastolic pressure plus one third of pulse pressure.

To determine mean pressure, diastolic pressure is considered more than the systolic pressure because diastolic period of cardiac cycle is longer (0.53 second) than systolic period (0.27 second).

Physiological Variations

1. Age

Arterial blood pressure increases as age advances.

2. Sex

In females, up to the period of menopause, arterial pressure is about 5 mm Hg less than in males of same age.

After menopause, the pressure in females becomes equal to that in males of same age.

3. Body Built

Pressure is more in obese persons than in lean persons.

4. Diurnal Variation

In early morning, the pressure is slightly low. It gradually increases and reaches the maximum at noon. It becomes low in evening.

5. After Meals

Arterial blood pressure is increased for few hours after meals due to increase in cardiac output.

6. During Sleep

Usually, pressure is reduced up to 15 to 20 mm Hg during deep sleep. However, it increases slightly during sleep associated with dreams.

7. Emotional Conditions

During excitement or anxiety, the blood pressure is increased due to release of adrenaline.

8. After Exercise

After moderate exercise, systolic pressure increases by 20 to 30 mm Hg above the basal level due to increase in force of contraction and stroke volume.

Normally, diastolic pressure is not affected by moderate exercise because the diastolic pressure depends upon peripheral resistance, which is not altered by moderate exercise.

After severe muscular exercise, systolic pressure rises by 40 to 50 mm Hg above the basal level.

But diastolic pressure reduces because the peripheral resistance decreases in severe muscular exercise.

Pathological Variations

Pathological variations in arterial blood pressure are:

• Hypertension
• Hypotension

Factors necessary for maintenance of normal arterial blood pressure are called local factors, mechanical factors or determinants of arterial blood pressure.

Local factors are divided into two types:

1. Central factors which are pertaining to the heart.
2. Peripheral factors which are pertaining to blood and blood vessels.

Central Factors

1. Cardiac Output

Systolic pressure is directly proportional to cardiac output.

Whenever cardiac output increases, the systolic pressure is increased, and when cardiac output is less, the systolic pressure is reduced.

Cardiac output increases in muscular exercise, emotional conditions, etc. So, in such conditions systolic pressure is increased.

In myocardial infarction, the cardiac output decreases resulting in fall in systolic pressure.

2. Heart Rate

Moderate changes in heart rate do not affect arterial blood pressure much.

However, marked alteration in heart rate affects blood pressure by altering cardiac output.

Peripheral Factors

1. Peripheral Resistance

Peripheral resistance is the resistance offered to blood flow at periphery. Resistance is offered at arterioles, which are called the resistant vessels.

Peripheral resistance plays an important role in maintaining diastolic pressure.

Diastolic pressure is directly proportional to peripheral resistance. When peripheral resistance increases, diastolic pressure increases and when peripheral resistance decreases, the diastolic pressure decreases.

2. Blood Volume

Blood pressure is directly proportional to blood volume.

Blood volume maintains the blood pressure through venous return and cardiac output.

If the blood volume increases, there is increase in venous return and cardiac output resulting in elevation of blood pressure.

3. Venous Return

Blood pressure is directly proportional to venous return.

When venous return increases, there is increase in ventricular filling and cardiac output resulting in elevation of arterial blood pressure.

4. Elasticity of Blood Vessels

Blood pressure is inversely proportional to the elasticity of blood vessels.

Due to elastic blood vessels, the vessels are distensible and are able to maintain the pressure.

When the elastic property is lost, blood vessels become rigid (arteriosclerosis) and pressure increases in elders.

Deposition of cholesterol, fatty acids and calcium ions cause rigidity of blood vessels (atherosclerosis) leading to increased blood pressure.

5. Velocity of Blood Flow

Pressure in a blood vessel is directly proportional to the velocity of blood flow.

If velocity of flow increases, resistance increases. So, blood pressure is increased.

6. Diameter of Blood Vessels

Arterial blood pressure is inversely proportional to diameter of the blood vessels.

If the diameter of blood vessels decreases, the peripheral resistance increases leading to increase in the pressure.

7. Viscosity of Blood

Arterial blood pressure is directly proportional to the viscosity of blood.

When viscosity of blood increases, peripheral resistance is increased and this increases the pressure.

Arterial blood pressure varies even under physiological conditions. However, immediately it is brought back to normal level because of the presence of well-organized regulatory mechanisms in the body.

Arterial blood pressure is maintained within normal limits by four types of regulatory mechanisms:

1. Nervous mechanism or short-term regulatory mechanism.
2. Renal mechanism or long-term regulatory mechanism.
3. Hormonal mechanism.
4. Local mechanism.

Nervous regulation is rapid among all the mechanisms involved in regulation of arterial blood pressure.

When blood pressure is altered, nervous system brings the pressure back to normal within few minutes.

Although nervous mechanism is quick in action, it operates only for a short period and then it adapts to the new pressure. Hence, it is called short-term regulation.

Nervous mechanism regulating the arterial blood pressure operates through vasomotor system.

Components of Vasomotor System

1. Vasomotor center.
2. Vasoconstrictor fibers.
3. Vasodilator fibers.

1. Vasomotor Center

Vasomotor center is bilaterally situated in reticular formation of medulla oblongata and lower part of pons.

Vasomotor center consists of three areas:

1. Vasoconstrictor area.
2. Vasodilator area.
3. Sensory area.

i. Vasoconstrictor Area

Vasoconstrictor area is also called pressor area. It forms the lateral portion of vasomotor center.

Vasoconstrictor area sends impulses to blood vessels through sympathetic vasoconstrictor fibers.

This area is also concerned with acceleration of heart rate.

ii. Vasodilator Area

Vasodilator area is also called depressor area. It forms the medial portion of vasomotor center.

This area suppresses the vasoconstrictor area and causes vasodilation. It is also concerned with inhibition of heart rate.

iii. Sensory Area

Sensory area is in nucleus of tractus solitarius, which is situated in the posterolateral part of medulla and pons.

This area receives sensory impulses via glossopharyngeal and vagal nerves from the periphery, particularly from the baroreceptors.

Sensory area in turn controls the vasoconstrictor and vasodilator areas.

2. Vasoconstrictor Fibers

Vasoconstrictor fibers belong to sympathetic division of autonomic nervous system.

These fibers cause vasoconstriction by release of the neurotransmitter noradrenaline.

3. Vasodilator Fibers

Vasodilator fibers are of three types:

1. Parasympathetic vasodilator fibers.
2. Sympathetic vasodilator fibers.
3. Antidromic vasodilator fibers.

i. Parasympathetic Vasodilator Fibers

Parasympathetic vasodilator fibers cause dilation of blood vessels by releasing the neurotransmitter acetylcholine.

ii. Sympathetic Vasodilator Fibers

Some of the sympathetic fibers cause vasodilation in certain areas by secreting acetylcholine.

Such fibers are called sympathetic vasodilator or sympathetic cholinergic fibers.

Sympathetic cholinergic fibers, which supply the blood vessels of skeletal muscles are important in increasing blood flow to muscles by vasodilation during conditions like exercise.

iii. Antidromic Vasodilator Fibers

Normally, impulses produced by a cutaneous receptor such as pain receptor pass through sensory nerve fibers.

Some of the impulses pass through other branches of axon and reach the blood vessels supplied by these branches.

These impulses dilate the blood vessels. It is called the antidromic or axon reflex. The nerve fibers are called antidromic vasodilator fibers.

Vasomotor Tone or Sympathetic Tone

Vasomotor tone or sympathetic tone is the continuous discharge of impulses from vasoconstrictor center through vasoconstrictor fibers.

Vasomotor tone plays an important role in regulating pressure by producing a constant partial state of constriction of the blood vessels.

Thus, arterial blood pressure is directly proportional to vasomotor tone. Vasomotor tone is also called sympathetic vasoconstrictor tone or sympathetic tone.

Mechanism of Action of Vasomotor Center

Vasomotor center regulates arterial blood pressure by causing vasoconstriction or vasodilation.

Its actions depend upon the impulses it receives from structures such as baroreceptors, chemoreceptors and respiratory centers.

Among these structures, baroreceptors have a major role in short-term regulation of blood pressure.

1. Baroreceptor Mechanism

Baroreceptors are the receptors which give response to change in blood pressure.

Baroreceptors are situated in carotid sinus and wall of aorta.

Role of Baroreceptors When Pressure Increases

When arterial blood pressure rises rapidly, baroreceptors are activated and send stimulatory impulses to nucleus of tractus solitarius through glossopharyngeal and vagal nerves.

Nucleus of tractus solitarius activates both vasoconstrictor and vasodilator areas of vasomotor center.

It inhibits vasoconstrictor area and excites the vasodilator area.

Inhibition of vasoconstrictor area causes reduction in vasomotor tone. Reduction in vasomotor tone causes vasodilation resulting in decreased peripheral resistance.

Simultaneous excitation of vasodilator center increases vagal tone. This decreases the rate and force of contraction of heart leading to reduction in cardiac output.

Both factors decrease peripheral resistance and reduce cardiac output, bringing arterial blood pressure back to normal level.

Role of Baroreceptors When Pressure Decreases

Fall in arterial blood pressure or occlusion of common carotid arteries decreases the pressure in carotid sinus.

This causes inactivation of baroreceptors.

The reduction in impulses from baroreceptors produces inhibition of the vasodilator center and stimulation of the vasoconstrictor center. Therefore, blood pressure rises.

2. Chemoreceptor Mechanism

Chemoreceptors are the receptors giving response to change in chemical constituents of blood.

Peripheral chemoreceptors are situated in carotid body and aortic body.

Function of Chemoreceptors

Peripheral chemoreceptors are sensitive to lack of oxygen and excess of carbon dioxide and hydrogen ion concentration in blood.

But lack of oxygen is the most potent stimulant for peripheral chemoreceptors.

When blood pressure decreases, blood flow decreases resulting in decreased oxygen content and excess of carbon dioxide and hydrogen ion.

These factors stimulate the chemoreceptors, which send impulses to vasomotor center. Blood pressure rises and blood flow increases.

Chemoreceptors play a major role in maintaining respiration rather than blood pressure.

Sinoaortic Mechanism and Buffer Nerves

Mechanism of action of baroreceptors and chemoreceptors of carotid and aortic region constitute sinoaortic mechanism.

Nerves from carotid and aortic regions are called buffer nerves because these nerves regulate heart rate, blood pressure and respiration.

3. Higher Centers

Vasomotor center is also controlled by impulses from two higher centers:

i. Cerebral Cortex

Area 13 in cerebral cortex is concerned with emotional reactions. During emotional conditions, this area sends impulses to vasomotor center.

Vasomotor center is activated, the vasomotor tone is increased and blood pressure rises.

ii. Hypothalamus

Stimulation of posterior and lateral nuclei of hypothalamus causes vasoconstriction and increases blood pressure.

Stimulation of preoptic area causes vasodilation and decrease in blood pressure.

Impulses from hypothalamus are mediated via vasomotor center.

4. Respiratory Centers

During the beginning of expiration, arterial blood pressure increases slightly, i.e. by 4 to 6 mm Hg.

It decreases during later part of expiration and during inspiration.

It is because of two factors:

1. Radiation of impulses from respiratory centers towards vasomotor center at different phases of respiratory cycle.
2. Pressure changes in thoracic cavity leading to alteration of venous return and cardiac output.

Kidneys play an important role in long-term regulation of arterial blood pressure.

When blood pressure alters slowly in several days/months/years, nervous mechanism adapts to altered pressure and loses the sensitivity for such conditions.

Renal mechanism alone can regulate the blood pressure. Therefore, it is called long-term regulation.

Kidneys regulate arterial blood pressure by two ways:

1. By regulation of ECF volume.
2. Through renin-angiotensin mechanism.

1. Regulation of Extracellular Fluid Volume

When blood pressure increases, kidneys excrete large amounts of water and salt, particularly by means of pressure diuresis and pressure natriuresis.

Pressure diuresis is the excretion of large quantity of water in urine because of increased blood pressure.

Even a slight increase in blood pressure doubles the water excretion.

Pressure natriuresis is the excretion of large quantity of sodium in urine because of increased blood pressure.

Because of diuresis and natriuresis, there is decrease in ECF volume and blood volume, which in turn brings the arterial blood pressure back to normal level.

When blood pressure decreases, reabsorption of water from renal tubules is increased.

This in turn increases ECF volume, blood volume and cardiac output resulting in restoration of blood pressure.

2. Through Renin-Angiotensin Mechanism

When blood pressure and ECF volume decrease, renin secretion from kidneys is increased.

Renin converts angiotensinogen into angiotensin I. Angiotensin I is converted into angiotensin II by angiotensin-converting enzyme (ACE).

Angiotensin II is converted into angiotensin III. It is converted into angiotensin IV.

Actions of Angiotensin II

When blood pressure and ECF volume decrease, renin secretion from kidneys is increased.

Angiotensin II acts in two ways to restore blood pressure.

i. Vasoconstriction

It causes constriction of arterioles in the body so that peripheral resistance is increased and blood pressure rises.

In addition, angiotensin II causes constriction of afferent arterioles in kidneys so that glomerular filtration reduces.

This results in retention of water and salts. This increases ECF volume and blood volume. This increases the blood pressure to normal level.

ii. Stimulation of Aldosterone Secretion

Simultaneously, angiotensin II stimulates adrenal cortex to secrete aldosterone.

This hormone increases reabsorption of sodium from renal tubules. Sodium reabsorption is followed by water reabsorption resulting in increased ECF volume and blood volume.

It increases the blood pressure to normal level.

Actions of Angiotensin III and Angiotensin IV

Like angiotensin II, angiotensins III and IV also increase the blood pressure and stimulate adrenal cortex to secrete aldosterone.

Many hormones are involved in the regulation of blood pressure. Hormones which increase or decrease arterial blood pressure are listed below.

In addition to nervous, renal and hormonal mechanisms, some local substances also regulate blood pressure.

Local substances regulate the blood pressure by vasoconstriction or vasodilation.

Local Vasoconstrictors

Local vasoconstrictor substances are of vascular endothelial origin and are known as endothelins (ET).

Endothelins are peptides with 21 amino acids.

Endothelins are produced by stretching of blood vessels.

Local Vasodilators

Local vasodilators are of two types:

1. Vasodilators of metabolic origin such as carbon dioxide, lactate, hydrogen ions and adenosine.
2. Vasodilators of endothelial origin such as nitric oxide (NO).

Local Substances Regulating Arterial Blood Pressure

Blood pressure is measured by direct and indirect methods.

Direct method is used in animals only. Indirect method is used in human beings as well as animals.

Apparatus: Mercury Sphygmomanometer

Apparatus used to measure blood pressure in human beings is called mercury sphygmomanometer.

Along with sphygmomanometer, stethoscope is also necessary to measure blood pressure.

Principle

When an external pressure is applied over the artery, blood flow through that artery is obstructed.

The pressure required to cause occlusion of blood flow indicates pressure inside the vessel.

Procedure

Brachial artery is usually chosen because of convenience.

Arm of sphygmomanometer is tied around upper arm, above the cubital fossa. Cuff should not be too tight or too loose. It is connected to sphygmomanometer.

Methods of Measuring Blood Pressure

Pressure can be measured by three methods:

1. Palpatory method.
2. Auscultatory method.
3. Oscillatory method.

1. Palpatory Method

First, the radial pulse is felt. While feeling the pulse, pressure is increased in the cuff by inflating air into it, with the help of a hand pump.

While doing this, mercury column shows pressure in the cuff.

When pressure is increased in the arm cuff, brachial artery is compressed and blood flow is obstructed. So, radial pulse disappears.

When radial pulse disappears, the pressure is further increased by about 20 mm Hg. Then pressure in cuff is slowly reduced by releasing the pressure of hand pump, i.e. cuff is deflated slowly.

This is done by feeling the pulse and simultaneously watching the mercury column in the apparatus.

Pressure is noted when the pulse reappears. Pressure at which pulse reappears indicates systolic pressure.

2. Auscultatory Method

Auscultatory method is the most accurate method to determine arterial blood pressure.

After determining systolic pressure in palpatory method, pressure in the cuff is raised by about 20 mm Hg above that level so that the brachial artery is occluded due to compression.

Now, stethoscope is placed over antecubital fossa and the arm cuff is slowly deflated.

While doing so, a series of sounds are heard through the stethoscope. These sounds are known as Korotkoff sounds.

Korotkoff sounds have five phases.

First Phase: Tapping Sound

While decreasing the pressure from arm cuff, occlusion of artery is relieved and when blood starts flowing through artery, first sound appears suddenly.

In a normal person, it appears when the pressure is reduced to 120 mm Hg. It is a clear tapping sound.

Appearance of tapping sound indicates systolic pressure.

Second Phase: Murmuring Sound

Following clear tapping sound, a soft murmuring sound is heard when the pressure is reduced further by about 15 mm Hg.

Third Phase: Gong Sound

After the murmuring sound, a very clear and louder gong sound is heard.

It is heard while reducing the pressure by another 15 mm Hg.

Fourth Phase: Muffled Sound

Next to the gong type sound, a mild and muffled sound is heard when pressure is decreased further by 5 mm Hg.

Fifth Phase: Disappearance of Sound

Muffling sound disappears. Disappearance of sound indicates diastolic pressure.

3. Oscillatory Method

When pressure in arm cuff is increased above the level of systolic pressure, the artery is occluded.

At this stage, mercury column in the manometer remains static.

When pressure is gradually reduced, some oscillations occur at the top of mercury column.

While deflating the cuff further, amplitude and duration of oscillations increase suddenly. It denotes systolic pressure.

When the cuff pressure is reduced further, amplitude and duration of oscillations is reduced. It reflects the diastolic pressure.

Because of its inaccuracy, this method is not followed in routine clinical practice.

By connecting the manometer to an appropriate recording device, oscillations of mercury column can be recorded graphically.

Other Types of Sphygmomanometers

Aneroid Sphygmomanometer

Aneroid sphygmomanometer consists of an aneroid device instead of mercury column.

It is commonly used in hospitals and clinics because of the concern of environmental toxicity of mercury.

However, aneroid sphygmomanometer is less accurate compared to mercury sphygmomanometer.

Automatic Digital Sphygmomanometer

Nowadays this type of blood pressure instrument is widely used.

This instrument has a microprocessor-driven air pump, which automatically inflates the cuff at a fixed pressure value.

Then, it releases the pressure oscillation pattern during the stepwise deflation.

This instrument determines the pulse rate also and results are shown on digital screen.

Automatic instruments do not need expert persons to measure the blood pressure since it has the same measuring facilities.

However, the accuracy of this instrument is controversial.

Pathological variations of arterial blood pressure are:

1. Hypertension.
2. Hypotension.

Hypertension

Hypertension is defined as the persistent high arterial blood pressure.

Clinically, when systolic pressure remains elevated above 140 mm Hg and diastolic pressure remains above 90 mm Hg, it is considered as hypertension.

If there is increase only in systolic pressure, it is called systolic hypertension.

Types of Hypertension

1. Primary hypertension.
2. Secondary hypertension.

1. Primary Hypertension or Essential Hypertension

Primary hypertension is the elevated blood pressure in the absence of any underlying disease. It is also called essential hypertension.

Arterial blood pressure is increased because of increased peripheral resistance which occurs due to some unknown cause.

2. Secondary Hypertension

Secondary hypertension is the high blood pressure due to some underlying disorders.

Different Forms of Secondary Hypertension

Hypotension is the low blood pressure.

When the systolic pressure is less than 90 mm Hg, it is considered as hypotension.

Types of Hypotension

1. Primary hypotension.
2. Secondary hypotension.

1. Primary Hypotension

Primary hypotension is the low blood pressure that develops in the absence of any underlying disease.

It is also called essential hypotension.

Frequent fatigue and weakness are the common symptoms of this condition.

However, the persons with primary hypotension are not easily susceptible to heart or renal disorders.

2. Secondary Hypotension

Secondary hypotension occurs due to some underlying diseases.

These include:

1. Myocardial infarction.
2. Hypoadrenalism.
3. Hypoactivity of pituitary gland.
4. Tuberculosis.
5. Nervous disorders.

Orthostatic Hypotension

Orthostatic hypotension is the sudden fall in blood pressure while standing for some time.

It is due to effect of gravity.

Gravity causes pooling of blood in lower limbs and decrease in blood pressure.

It develops in persons affected by myasthenia gravis or some nervous disorders like tabes dorsalis, syringomyelia and diabetic neuropathy.

Common symptom of this condition is orthostatic syncope.